SEARCH · Search PubMed

Results for “MESENTERIC VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,603 records · Page 89Linked to original sources

PubMed1998

Vascular responses of isolated mesenteric resistance and basilar arteries from short- and long-term diabetic rats.

Vascular dysfunctions, e.g. alterations in the reactivity of blood vessels to neurotransmitters and hormones, are a well-established complication of diabetes mellitus. Whether these impairments are a consequence of direct postsynaptic deficits and/or indirect presynaptic deficits remains to be determined. To this end, we investigated the influence of the duration of diabetes on relaxation and contraction responses of isolated mesenteric resistance and equally-sized basilar arteries to postsynaptic activation by various vasoactive agents, using streptozotocin-induced diabetic rats and age-matched controls. Relaxation responses to vasodilator agents were studied in KCl-precontracted arteries. The duration of diabetes (4 or 40 weeks) did not affect the vasodilator responses to sodium nitroprusside or salbutamol in either artery. In mesenteric resistance vessels from short-term (4 weeks) and long-term (40 weeks) diabetic rats the vasoconstrictor responses to KCI, serotonin and vasopressin were the same as those in non-diabetic rats; however, the sensitivity (EC50) to noradrenaline was slightly but significantly enhanced after the long-term diabetic state. In contrast to the mesenteric arteries, noradrenaline did not cause contraction in basilar arteries taken from diabetic and control rats. Thus, there appear to be important differences in the reactivity to noradrenaline of the peripheral and cerebral vasculature. The basilar artery from short-term and long-term diabetic rats did not show different responsiveness to vasopressin whereas to serotonin a significant enhanced and decreased sensitivity (EC10 and EC50) was demonstrated in short-term and long-term diabetes, respectively. Our findings indicate that postsynaptic impairments do not play a major role in the alterations of vasoreactivity to vasodilators, noradrenaline or vasopressin seen in experimental diabetes. However, the duration of the diabetic state may have serious consequences for vasoreactivity of basilar arteries to serotonin and, therefore, warrants further investigations.

Animals↗

PubMed2001

Responses of fetal ovine systemic and umbilical arteries to angiotensin II.

Angiotensin II (ANG II) contracts umbilical arteries and has been hypothesized to regulate fetal blood pressure primarily by altering umbilical vascular resistance. To determine whether systemic arteries in term fetal sheep are sensitive to ANG II, isometric contraction of endothelium-intact isolated fetal renal, mesenteric, and umbilical arteries in response to ANG II was studied. ANG II (10(-7) M) elicited contractile responses in all three vessels (43 +/- 8%, 99 +/- 21%, and 105 +/- 5% of the maximal response seen with 90 mM KCl for renal, mesenteric, and umbilical arteries, respectively). The time course of the contractile responses differed among the vessels: renal and mesenteric arteries exhibited rapid transient contraction followed by relaxation, whereas umbilical artery displayed a more slowly developing but sustained contraction (1 +/- 0%, 3 +/- 1%,and 93 +/- 4% of maximal contractile response at 5 min, for renal, mesenteric, and umbilical arteries, respectively). The AT1 receptor antagonist, losartan (10(-6) M), abolished contractile responses in renal and mesenteric arteries but only slowed the contraction in umbilical artery in response to ANG II and had no effect on maximal tension. AT2 receptor blockade (PD 123319, 10(-7) M) had no significant effect on the response to ANG II in any vessel. Indomethacin (10(-6) M) significantly potentiated contraction to ANG II in renal and mesenteric but not umbilical arteries. Northern and Western blot analyses demonstrated the presence of AT1 mRNA and protein in all three vessels. Immunostaining for the AT1 receptor was present in endothelium and the tunica media. These findings demonstrate the AT1 receptor is present and functionally active in fetal systemic arteries and are consistent with previous findings that the umbilical circulation displays a greater responsiveness to ANG II than the systemic vasculature.

Angiotensin II↗

PubMed1992

Effects of interleukin-1 receptor antagonist on three types of responses to interleukin-1 in rabbit isolated blood vessels.

Interleukin-1 receptor antagonist (IRA) is a secretory product of human monocytes or related cell lines that acts as a pure interleukin-1 (IL-1) antagonist in several bioassays. IRA administration was reportedly a life-saving intervention in rabbits injected with lethal doses of bacterial lipopolysaccharide (LPS). We report the inhibitory effect of IRA on three distinct types of vascular responses to IL-1 in rabbit isolated blood vessels. The rabbit isolated superior mesenteric artery, when precontracted with phenylephrine, relaxed in a sustained manner in less than 30 min following application of recombinant interleukin-1 beta (12-290 pM), and this was a prostaglandin (PG)-dependent and endothelium-independent process. IRA (human recombinant sequence; 0.9-15 nM) behaved as an antagonist of IL-1 alpha or IL-1 beta, based on the surmountability and the concentration dependence, but could only prevent the effect of IL-1, not reverse it. IRA had no direct effect on the preparation and did not influence the acute relaxing effect elicited by substance P or iloprost, a PGI2 mimetic. Exposure to IL-1 beta depressed the response to noradrenaline (NA) in several hours in rabbit aorta rings. The inhibitory effect of IL-1 beta was endothelium and prostaglandin independent, but was prevented by a treatment with NG-nitro-L-arginine (a nitric oxide synthesis inhibitor), cycloheximide, dexamethasone, or IRA. Using the residual NA-induced contraction as a quantification of the IL-1 agonist effect, IRA was a very potent antagonist of IL-1 beta but was not totally surmountable.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Embolization of superior mesenteric artery branches in dogs. Ischemic bowel changes depend on location of vessel occlusion and embolic materials.

OBJECTIVE: To evaluate the degree of ischemic changes of the small intestine after arterial embolization of proximal or distal arteries with Gelfoam particles and coils in dogs. METHODS: Superselective arterial embolization in 18 dogs was performed using a coaxial catheter system. Gelfoam occlusion of the proximal level of ileal or jejunal arteries was performed in four dogs (group A). Gelfoam occlusion of the distal level was performed in four dogs (group B). Coil occlusion of the proximal level was performed in five dogs (group C). Coil occlusion of the distal level was performed in five dogs (group D). All 18 dogs were killed 1 day after the procedure. Gross and microscopic findings were evaluated. RESULTS: The embolizations were successful in all dogs. In group B, significant mucosal destruction, lymphocyte proliferation of the submucosa and mucosa, and diffuse swelling in all layers of the intestine were found in all four dogs. Three revealed diffuse ischemic changes and one showed focal ischemic changes. In groups A and C, all the layers of the intestine were intact and did not show any ischemic changes. In group D, one dog showed erosion of a small portion of mucosa and lymphocytic infiltration. The other dogs showed nonspecific findings in all layers of the intestine. CONCLUSIONS: Proximal embolization with Gelfoam and coils as well as distal embolization with coils did not cause ischemia. However, ischemic changes in the intestinal wall could be observed after distal embolization with Gelfoam.

Angiography↗

PubMed1997

Endothelium and cannabinoid receptor involvement in levcromakalim vasorelaxation.

Levcromakalim was more potent at relaxing rat small mesenteric arteries with endothelium (EC50, 84+/-10 nM) than denuded vessels (EC50, 779+/-101 nM). The cannabinoid receptor antagonist SR 141716A (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H-pyrazole-3-carboxamide hydrochloride; 1 microM) shifted the levcromakalim concentration/response curve 7.6-fold rightwards in intact vessels but had no effect in de-endothelialised vessels. Similar effects occurred with pinacidil. Combination of the K+ channel blockers apamin (1 microM) and charybdotoxin (100 nM) shifted the levcromakalim concentration/response curve 3-fold rightwards only in intact vessels. It is concluded that levcromakalim and pinacidil relax mesenteric arteries partly by releasing a relaxing factor from endothelium, possibly an endogenous cannabinoid.

Animals↗

PubMedDate not supplied

[A case of aneurysm of the celiac trunk ruptured into the duodenum].

A case of repeated, exsanguinating gastrointestinal haemorrhage in a 36-yr-old man, due to rupture in the duoedenum of an arteriosclerotic aneurysm of the coeliac artery, is described. Selective arteriography enabled the cause of bleeding to be established. The pictures for the coeliac and superior mesenteric arteries showed good hepatic arterial vascularisation via the vessels issuing from the right hand side of the superior mesenteric, immediately after its point of origin. Successful aneurysmectomy was not performed until the fifth operation, when the cause of bleeding had thus been made clear.

Adult↗

PubMed1993

[The restitution of the population of the mesenteric mast cells of the rat intestine].

Reparative processes in rat mesentery mast cells after their depletion by injection of distilled water were studied. In accordance with mast cell localization common population was divided into two subpopulations: paravascular and membranous located in a zone free from blood vessels. Only membranous subpopulation localized in "mesenteric windows" was destroyed by hypo-osmia. At the same time paravascular mast cells were not destroyed. Destructive processes in membranous zones were associated with an increase in the number of paravascular mast cells. Subsequent gradual colonization of mesenteric areas destroyed by distilled water resulted in decrease in the number of mast cell associations along blood vessels. A similar inversely proportional relationship between mast cell count in vessel-free zones and number of mast cell associations near blood vessels was observed in intact mesentery as well. We suppose that the processes of violent destruction of rat mesentery mast cells as well as their natural death stimulate a compensatory increase of their counts in paravascular zones.

Animals↗

PubMed2001

Effect of the blood substitute diaspirin crosslinked hemoglobin in rat mesenteric and human radial collateral arteries.

The actions of the blood substitute diaspirin crosslinked hemoglobin (DCLHb) were investigated in rat (small mesenteric artery) and human (radial collateral artery) resistance vessels mounted in a wire myograph for isometric tension recording. DCLHb did not contract resting vessels from rats, but vasoconstrictor responses were observed in isolated arteries and perfused mesenteric beds prestimulated with threshold concentrations of methoxamine. The DCLHb contractile responses were greatly attenuated by N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) or endothelial removal, whereas BQ-123 (endothelin A receptor antagonist), prazosin (alpha1-adrenoceptor antagonist), or indomethacin (cyclooxygenase inhibitor) had no effect. Endothelium-dependent relaxations to carbachol in both rat mesenteric and human radial collateral artery were inhibited by DCLHb. Relaxations to carbachol were studied in the presence of L-NAME or 25 mM KCl to investigate the effect of DCLHb on endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide, respectively. In both rat and human vessels, EDHF-mediated relaxations were not affected by DCLHb preincubation, whereas the nitric oxide component of carbachol-induced relaxations was practically abolished. In conclusion, inhibition of the effects of basal nitric oxide release underpins the vasoconstrictor effects of DCLHb. DCLHb effectively abolishes the nitric oxide component of carbachol-induced relaxation, with no effect on the EDHF-mediated component in both isolated rat mesenteric and human radial collateral arteries.

Animals↗

PubMed1993

Effects of oral alcohol on superior mesenteric artery blood flow in normal man, horizontal and tilted.

1. The cardiovascular effects of oral alcohol (0.5 g/kg body weight diluted to 300 ml in sugar-free orange juice) were compared with those of placebo in 10 normal subjects. Measurements were made while the subjects were supine and horizontal for 45 min and after 10 min of 45 degrees head-up tilt. 2. After alcohol, plasma alcohol levels rose from 1.9 +/- 1.3 to 61.6 +/- 6.5 mg/100 ml. After placebo, plasma alcohol levels did not increase. After alcohol and placebo, supine blood pressure was unchanged; heart rate, both supine and during tilt, rose after alcohol only. 3. After alcohol, superior mesenteric artery and digital skin blood flow increased and calculated vascular resistances fell. There was no change after placebo. 4. Forearm blood flow, forearm vascular resistance and cardiac index did not change in either phase, except for a fall in cardiac index during tilt but only after alcohol. 5. In conclusion, the acute ingestion of 0.5 g of alcohol/kg body weight in normal subjects raised heart rate and actively dilated the superior mesenteric artery and digital skin vessels. There was no effect on blood pressure, cardiac output and skeletal muscle vascular tone. During head-up tilt after alcohol, there was a tendency for blood pressure to fall with a compensatory rise in heart rate.

Adult↗

PubMed2002

Canine mesenteric artery and vein convey no difference in the content of major contractile proteins.

BACKGROUND: Mesenteric arteries and veins are composed of tonic smooth muscles and serve distinct functions in the peripheral circulation. However, the basis for the functional disparity of the resistive and capacitative parts of the mesenteric circulation is poorly understood. We studied potential differences in the expression levels of six contractile proteins in secondary and tertiary branches of the inferior mesenteric artery and vein along with differences in the vessel wall morphology. RESULTS: Bright field and electron microscopy showed that both vessel walls had the same major structural elements. The arterial walls, however, had greater number, and more tightly assembled, smooth muscle cell layers compared to vein walls. The content of actin, myosin heavy chain, myosin light chain, and calponin was similar in the two blood vessels. The artery expressed higher amount of the actin-binding protein caldesmon than the vein (41.86 +/- 2.33 and 30.13 +/- 3.37 microg/mg respectively, n = 12). Although the total tropomyosin content was almost identical in both blood vessels, the alpha isoform dominated in the artery, while the beta isoform prevailed in the vein. CONCLUSIONS: Canine mesenteric artery and vein differ in vessel wall morphology but do not convey differences in the expression levels of actin, myosin light chain, myosin heavy chain and calponin. The two vascular networks express distinct amounts of caldesmon and tropomyosin, which might contribute to the fine tuning of the contractile machinery in a manner consistent with the physiological functions of the two vascular networks.

Actins↗

PubMed1980

Toxic megacolon due to ischemic enterocolitis associated with retroperitoneal fibrosis.

A 46-yr-old man, in whom retroperitoneal fibrosis had been found 4 yr previously, presented with abdominal pain, fever, diarrhea, and marked dilation of the transverse colon with superficial ulceration. The megacolon was unresponsive to nasogastric suction, corticosteroids, antibiotics, and total parenteral nutrition. Arteriograms revealed total occlusion of the celiac axis and superior and inferior mesenteric arteries. Laparotomy showed encasement of the retroperitoneal vessels by dense fibrous tissue. A vascular bypass graft was performed, connecting the distal superior mesenteric artery to the right external iliac artery. This led to complete and lasting resolution of gastrointestinal complaints.

Aortography↗

PubMedDate not supplied

The portal vein and its main affluents. An anatomic and morphometric study.

There are reported the results of certain measurements made on 158 human cadavers of both sexes. A series of main parameters are given, such as the distance between the superior mesenteric vein and on the one hand its confluence with other vessels and on the other hand the pancreas and the horizontal part of the duodenum: the distance between the superior mesenteric vein together with the portal vein, and the inferior caval vein; the diameters of the portal trunk and the confluence angle between the roots of the portal vein. The results reflect the possibility to perform a troncular portocaval anastomosis in at least 90 per cent of the cases. The authors' attention was, however, directed towards the anatomy of the superior mesenteric vein, as this vessel is preferred by some surgeons in the achievement of the portocaval anastomosis.

Female↗

PubMed1995

Effects of long-term treatment with angiotensin-converting enzyme inhibitor on angiotensin II and prostacyclin release from mesenteric arteries in spontaneously hypertensive rats.

To evaluate the long-term effects of an angiotensin-converting enzyme inhibitor (ACEI) on vascular angiotensin II (AII), eicosanoid production and vascular reactivities, we treated spontaneously hypertensive rats (SHR) with alacepril for 6 weeks and perfused the isolated mesenteric arterial bed which contains resistance vessels. Alacepril significantly lowered the arterial blood pressure. Changes in perfusion pressure in response to norepinephrine (NE) were attenuated, and isoproterenol-stimulated AII release from the perfused mesenteric arterial beds was inhibited in the alacepril-treated SHR. Vasodilation induced by acetylcholine (Ach) and prostacyclin (PGI2) release was significantly increased in the vasculature of the alacepril-treated SHR. Alacepril exerted no effect on cyclic GMP (cGMP) formation, but increased cAMP formation in the vasculature. These findings suggest that ACEI inhibits AII formation and facilitates PGI2 production in the resistance vessels, which leads to blunting of the pressor response to NE and improvement of endothelial function in SHR. These humoral and mechanical changes in the vasculature may contribute to the depressor and organ protective effects of ACEI.

Acetylcholine↗

PubMed2001

[Multislice spiral CT angiography in the evaluation of the anatomy of splanchnic vessels: preliminary experience].

PURPOSE: The aim of this study was to optimize the protocol for multislice spiral CT angiography and to assess the ability of the technique to detect the anatomy of splanchnic vessels, using volume rendering as reconstruction algorithm. MATERIAL AND METHODS: The anatomy of splanchnic vessels was studied in 19 patients (11 men, 8 women, age range 38-83 years) undergoing CT of the abdomen and pelvis. All examinations were performed with a multislice spiral CT scanner (Somatom Plus 4 Volume Zoom; Siemens, Erlangen, Germany) using the following parameters: collimation, 1 mm; slice width, 1 mm; table feed, 8 mm/sec; reconstruction interval, 1 mm; mAs, 120; kVp, 120. Before the study, the patients received 800 ml of water as oral contrast agent to opacify the stomach and small bowel. A nonionic contrast medium (130-140 ml; Xenetix 350, Guerbet, Aulnay-Sous-Bois, France) was infused intravenously at a rate of 3-5 ml/sec. Two scans of the abdomen and pelvis were obtained at 20-25 sec (arterial phase) and 60-65 sec (venous phase) after starting contrast medium injection. Image elaboration was performed using Vitrea 2.2 (Vital Images; Minneapolis, Minn., USA), a software with volume-rendering capabilities. RESULTS: All major arterial (celiac trunk, superior mesenteric artery, and inferior mesenteric artery) and venous (portal vein, superior mesenteric vein, inferior mesenteric vein, and splenic vein) vessels could be evaluated with excellent detail in all patients. Side branches, including small collaterals, could also be easily visualized. Volume rendered images always provided better understanding of the 3D anatomic relationships among splanchnic vessels and surrounding organs. DISCUSSION AND CONCLUSIONS: Multislice spiral CT angiography allows for optimal depiction of the anatomy of splanchnic vessels. It can be anticipated that the clinical applications of this imaging modality in the study of splanchnic vessels will be greatly expanded. However, further studies are necessary to rigorously compare the results of multislice spiral CT angiography with conventional angiography in terms of diagnostic accuracy.

Adult↗

PubMed1988

Ketanserin decreases sympathetic nervous activity in hypertension.

This study was performed to investigate whether ketanserin (a serotonergic receptor antagonist) might affect the sympathetic nerve activity in resistance vessels of hypertension. Isolated perfused mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHRS, Okamoto and Aoki, 20-22 weeks old) and age-matched Wistar Kyoto rats (WKY), and effects of ketanserin on norepinephrine overflow from the adrenergic nerve endings as well as on vascular responsiveness were examined. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited by ketanserin, in a dose-dependent manner. Norepinephrine overflow during electrical nerve stimulation was also suppressed by ketanserin. Inhibitory degrees of pressor responses and norepinephrine overflow during electrical nerve stimulation by ketanserin were significantly greater in SHRs than those in WKY rats. These results suggest that ketanserin could affect presynaptic neurotransmitter release from the adrenergic nerve endings in resistance vessels. These sympatho-depressive actions might contribute, at least partially, to the hypotensive mechanisms of ketanserin.

Animals↗

PubMed2006

Mesenteric vascular responsiveness in a rat model of pregnancy-induced hypertension.

Reduced perfusion to the placenta in early pregnancy is believed to be the initiating factor in the development of preeclampsia, triggering local ischemia and systemic vascular hyperresponsiveness. This sequence of events creates a predisposition to the development of altered vascular function and hypertension. This study was designed to determine the influence of placental insufficiency on the responsiveness of mesenteric resistance arteries in an animal model of preeclampsia. Placental insufficiency was induced by reduction in uteroplacental perfusion pressure (RUPP) in experimental Sprague-Dawley rat dams. The uterine branches of the ovarian arteries and the abdominal aortae of pregnant rats were surgically constricted on gestational Day 14. Dams in the control group underwent a sham procedure. Rats were euthanized on gestational Day 20, followed by removal of the small intestine and adjacent mesentery. First-order mesenteric resistance arteries were mounted on a small vessel wire myograph and challenged with incremental concentrations of vasoconstrictors and vasorelaxants. Mesenteric arteries in dams with placental insufficiency demonstrated an increased maximal tension to phenylephrine (7.15 +/- 0.15 vs. 5.4 +/- 0.27 mN/mm, P < 0.001); potassium chloride at 60 mM (3.43 +/- 0.11 vs. 2.77 +/- 0.14 mN/mm, P < 0.01) and 120 mM (3.92 +/- 0.18 vs. 2.97 +/- 0.16 mN/mm, P < 0.01); and angiotensin II (2.59 +/- 0.42 vs. 1.51 +/- 0.22 mN/mm, P < 0.05). Maximal relaxation to endothelium-dependent relaxants acetylcholine and calcium ionophore (A23187) was not significantly reduced. Data suggest that placental insufficiency leads to hyperresponsiveness to vasoconstrictor stimuli in mesenteric arteries.

Animals↗

PubMed1985

Synthetic atrial natriuretic factor is a specific dilator of noradrenaline and serotonin activated renal resistance vessels.

The action of a synthetic 'atrial natriuretic factor' (sANF) on induced tone in isolated rat renal resistance vessels (lumen diameter about 200 microns) was examined and compared with the effects of sANF on resistance vessels of similar size taken from the cerebral, mesenteric and femoral vasculature. Synthetic ANF caused a relaxation of the renal vessels when these were submaximally activated with noradrenaline or serotonin, but had no effect on the responses of the other vessels to these agonists. In contrast to previous reports concerning rabbit aortic vessels, methylene blue (which is thought to cause inhibition of guanyl cyclase) did not reduce the dilator response to sANF in the renal vessels. The results demonstrate that sANF has a specific relaxing effect on renal resistance vessels, and are consistent with its effect being mediated through specific receptors. The mechanism of this relaxant effect remains unknown.

Animals↗

PubMed2002

Endothelial nitric oxide modulates perivascular sensory neurotransmission in the rat isolated mesenteric arterial bed.

1. A possible role of nitric oxide (NO) as a modulator of capsaicin-sensitive sensory neurotransmission in blood vessels was investigated in the rat isolated mesenteric arterial bed. 2. Electrical field stimulation (EFS) of methoxamine-preconstricted mesenteric beds elicited frequency-dependent vasorelaxation mediated by capsaicin-sensitive sensory nerves. N(G)-nitro-L-arginine methyl ester (L-NAME, 10 and 300 microM) and 7-nitroindazole (7-NI, 100 microM), inhibitors of nitric oxide synthase (NOS), augmented sensory neurogenic vasorelaxation. D-NAME (300 microM), 6-aminoindazole (100 microM) and N(omega)-propyl-L-arginine (50 nM), a selective inhibitor of neuronal NOS, were without effect. The effect of 10 microM L-NAME was reversed by L-arginine (1 mM), the substrate for NOS. 3. L-NAME (300 microM) and 7-NI (100 microM) had no significant effect on vasorelaxations to calcitonin gene-related peptide (CGRP), the principal motor neurotransmitter of capsaicin-sensitive sensory nerves in rat mesenteric arteries, or to capsaicin, indicating a prejunctional action. The inhibitors of NOS had no effect on vasorelaxation to forskolin, but augmented vasorelaxation to sodium nitroprusside (SNP). 4. Removal of the endothelium augmented sensory neurogenic vasorelaxation, but did not affect vasorelaxation to CGRP, indicating a prejunctional action of endothelial NO. 5. In the absence of endothelium, L-NAME (300 microM) inhibited, and 7-NI (100 microM) caused no further augmentation of sensory neurotransmission. 6. SNP (100 nM), a nitric oxide donor, attenuated sensory neurogenic relaxations to EFS. 7. In rat isolated thoracic aortic rings, L-NAME (100 microM) and 7-NI (100 microM) attenuated concentration-dependent relaxations to acetylcholine. 8. These data show that NO modulates sensory neurotransmission evoked by EFS of the rat isolated mesenteric arterial bed, and that when NO synthesis is blocked sensory neurogenic relaxation is augmented. The source of NO is the vascular endothelium.

Animals↗